Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans.

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.     

Relationship between pulmonary O2 uptake kinetics and muscle deoxygenation during moderate-intensity exercise.

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (Vo -->Vo2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 +/- 3 yr; mean +/- SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath Vo2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 Vo2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for Vo2p (30 +/- 8 s) was slower (P < 0.01) than that for HHb (10 +/- 3 s). The TDHHb before an increase in HHb was 13 +/- 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 Vo2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.     

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

O2 uptake kinetics, pyruvate dehydrogenase activity, and muscle deoxygenation in young and older adults during the transition to moderate-intensity exercise

The adaptation of pulmonary O(2) uptake (Vo(2)(p)) kinetics is slowed in older compared with young adults during the transition to moderate-intensity exercise. In this study, we examined the relationship between Vo(2)(p) kinetics and mitochondrial pyruvate dehydrogenase (PDH) activity in young (n = 7) and older (n = 6) adults. Subjects performed cycle exercise to a work rate corresponding to approximately 90% of estimated lactate threshold. Phase 2 Vo(2)(p) kinetics were slower (P < 0.05) in older (tau = 40 +/- 17 s) compared with young (tau = 21 +/- 6 s) adults. Relative phosphocreatine (PCr) breakdown was greater (P < 0.05) at 30 s in older compared with young adults. Absolute PCr breakdown at 6 min was greater (P < 0.05) in older compared with young adults. In young adults, PDH activity increased (P < 0.05) from baseline to 30 s, with no further change observed at 6 min. In older adults, PDH activity during baseline exercise was similar to that seen in young adults. During the exercise transition, PDH activity did not increase (P > 0.05) at 30 s of exercise but was elevated (P < 0.05) after 6 min. The change in deoxyhemoglobin (HHb) was greater for a given Vo(2)(p) in older adults, and there was a similar time course of HHb accompanying the slower Vo(2)(p) kinetics in the older adults, suggesting a slower adaptation of bulk O(2) delivery in older adults. In conclusion, the slower adaptation of Vo(2)(p) in older adults is likely a result of both an increased metabolic inertia and lower O(2) availability.     

Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.     

Prior heavy-intensity exercise speeds VO2 kinetics during moderate-intensity exercise in young adults.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.     

Effect of age on O(2) uptake kinetics and the adaptation of muscle deoxygenation at the onset of moderate-intensity cycling exercise.

Phase 2 pulmonary O(2) uptake (Vo(2(p))) kinetics are slowed with aging. To examine the effect of aging on the adaptation of Vo(2(p)) and deoxygenation of the vastus lateralis muscle at the onset of moderate-intensity constant-load cycling exercise, young (Y) (n = 6; 25 +/- 3 yr) and older (O) (n = 6; 68 +/- 3 yr) adults performed repeated transitions from 20 W to work rates corresponding to moderate-intensity (80% estimated lactate threshold) exercise. Breath-by-breath Vo(2(p)) was measured by mass spectrometer and volume turbine. Deoxy (HHb)-, oxy-, and total Hb and/or myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). Vo(2(p)) data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb data were filtered and averaged to 5-s bins. Vo(2(p)) data were fit with a monoexponential model for phase 2, and HHb data were analyzed to determine the time delay from exercise onset to the start of an increase in HHb and thereafter were fit with a single-component exponential model. The phase 2 time constant for Vo(2(p)) was slower (P < 0.01) in O (Y: 26 +/- 7 s; O: 42 +/- 9 s), whereas the delay before an increase in HHb (Y: 12 +/- 2 s; O: 11 +/- 1 s) and the time constant for HHb after the time delay (Y: 13 +/- 10 s; O: 9 +/- 3 s) were similar in Y and O. However, the increase in HHb for a given increase in Vo(2(p)) (Y: 7 +/- 2 microM x l(-1) x min(-1); O: 13 +/- 4 microM x l(-1) x min(-1)) was greater (P < 0.01) in O compared with Y. The slower Vo(2(p)) kinetics in O compared with Y adults was accompanied by a slower increase of local muscle blood flow and O(2) delivery discerned from a faster and greater muscle deoxygenation relative to Vo(2(p)) in O.     

O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise

Inhibition of carbonic anhydrase (CA) isassociated with a lower plasma lactate concentration([La]_pl)during fatiguing exercise. We hypothesized that a lower[La]_plmay be associated with faster O₂uptake (O₂) kinetics during constant-load exercise. Seven men performed cycle ergometer exercise during control (Con) and acute CA inhibition with acetazolamide (Acz,10 mg/kg body wt iv). On 6 separate days, each subject performed 6-minstep transitions in work rate from 0 to 100 W (below ventilatory threshold,<ET)or to a O₂ corresponding to~50% of the difference between the work rate atET and peakO₂(>ET).Gas exchange was measured breath by breath. Trials were interpolated at1-s intervals and ensemble averaged to yield a single response. The mean response time (MRT, i.e., time to 63% of total exponential increase) for on- and off-transients was determined using a two- (<ET) or athree-component exponential model(>ET).Arterialized venous blood was sampled from a dorsal hand vein andanalyzed for[La]_pl.MRT was similar during Con (31.2 ± 2.6 and 32.7 ± 1.2 s for onand off, respectively) and Acz (30.9 ± 3.0 and 31.4 ± 1.5 s for on and off, respectively) for work rates<ET. Atwork rates >ET, MRTwas similar between Con (69.1 ± 6.1 and 50.4 ± 3.5 s for on andoff, respectively) and Acz (69.7 ± 5.9 and 53.8 ± 3.8 s for on and off, respectively). On- and off-MRTs were slower for>ET thanfor <ETexercise.[La]_plincreased above 0-W cycling values during<ET and>ET exercise but was lower at the end of the transition during Acz (1.4 ± 0.2 and 7.1 ± 0.5 mmol/l for<ET and>ET,respectively) than during Con (2.0 ± 0.2 and 9.8 ± 0.9 mmol/lfor <ETand >ET,respectively). CA inhibition does not affectO₂ utilization at the onset of<ET or>ETexercise, suggesting that the contribution of oxidative phosphorylationto the energy demand is not affected by acute CA inhibition with Acz.

     

Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise.

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.     

Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.     

Prior exercise speeds pulmonary O2 uptake kinetics by increases in both local muscle O2 availability and O2 utilization.

The effect of prior exercise on pulmonary O(2) uptake (Vo(2)(p)), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Delta50%, 8 min; HVY 2) KE exercise. Vo(2)(p) was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O(2)Hb)-, deoxy (HHb)-, and total (Hb(tot)) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 Vo(2)(p), LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb - MRT = TD + tau) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 Vo(2)(p) kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the Vo(2)(p) slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O(2)Hb and Hb(tot) were elevated throughout the on-transient following prior heavy-intensity exercise. The tauLBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 microM (10); HVY 2: 25 microM (10); P < 0.001] and the HHb-to-Vo(2)(p) ratio [(HHb/Vo(2)(p)) HVY 1: 14 microM x l(-1) x min(-1) (6); HVY 2: 17 microM x l(-1) x min(-1) (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 tauVo(2)(p) was the result of both elevated local O(2) availability and greater O(2) extraction evidenced by the greater HHb amplitude and HHb/Vo(2)(p) ratio following prior heavy-intensity exercise.     

Effect of L-NAME on oxygen uptake kinetics during heavy-intensity exercise in the horse.

There is evidence that oxidative enzyme inertia plays a major role in limiting/setting the O(2) uptake (VO(2)) response at the transition to higher metabolic rates and also that nitric oxide (NO) competitively inhibits VO(2) within the electron transport chain. To investigate whether NO is important in setting the dynamic response of VO(2) at the onset of high-intensity (heavy-domain) running in horses, five geldings were run on a treadmill across speed transitions from 3 m/s to speeds corresponding to 80% of peak VO(2) with and without nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor (20 mg/kg; order randomized). L-NAME did not alter (both P > 0.05) baseline (3 m/s, 15.4 +/- 0.3 and 16.2 +/- 0.5 l/min for control and L-NAME, respectively) or end-exercise VO(2) (56.9 +/- 5.1 and 55.2 +/- 5.8 l/min for control and L-NAME, respectively). However, in the L-NAME trial, the primary on-kinetic response was significantly (P < 0.05) faster (i.e., reduced time constant, 27.0 +/- 2.7 and 18.7 +/- 3.0 s for control and L-NAME, respectively), despite no change in the gain of VO(2) (P > 0.05). The faster on-kinetic response was confirmed independent of modeling by reduced time to 50, 63, and 75% of overall VO(2) response (all P < 0.05). In addition, onset of the VO(2) slow component occurred earlier (124.6 +/- 11.2 and 65.0 +/- 6.6 s for control and L-NAME, respectively), and the magnitude of the O(2) deficit was attenuated (both P < 0.05) in the L-NAME compared with the control trial. Acceleration of the VO(2) kinetics by L-NAME suggests that NO inhibition of mitochondrial VO(2) may contribute, in part, to the intrinsic metabolic inertia evidenced at the transition to higher metabolic rates in the horse.     

Muscle chemoreflex elevates muscle blood flow and O2 uptake at exercise onset in nonischemic human forearm.

We tested the hypothesis that increases in forearm blood flow (FBF) during the adaptive phase at the onset of moderate exercise would allow a more rapid increase in muscle O2 uptake (VO2 mus). Fifteen subjects completed forearm exercise in control (Con) and leg occlusion (Occ) conditions. In Occ, exercise of ischemic calf muscles was performed before the onset of forearm exercise to activate the muscle chemoreflex evoking a 25-mmHg increase in mean arterial pressure that was sustained during forearm exercise. Eight subjects who increased FBF during Occ compared with Con in the adaptation phase by >30 ml/min were considered "responders." For the responders, a higher VO2 mus accompanied the higher FBF only during the adaptive phase of the Occ tests, whereas there was no difference in the baseline or steady-state FBF or VO2 mus between Occ and Con. Supplying more blood flow at the onset of exercise allowed a more rapid increase in VO2 mus supporting our hypothesis that, at least for this type of exercise, O2 supply might be limiting.     

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.     

Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise

We used anexercise paradigm with repeated bouts of heavy forearm exercise to testthe hypothesis that alterations in local acid-base environment thatremain after the first exercise result in greater blood flow andO₂ delivery at the onset of the second bout of exercise.Two bouts of handgrip exercise at 75% peak workload were performed for5 min, separated by 5 min of recovery. We continuously measured bloodflow using Doppler ultrasound and sampled venous blood forO₂ content, PCO₂, pH, and lactateand potassium concentrations, and we calculated muscle O₂uptake (O₂). Forearm blood flow waselevated before the second exercise compared with the first andremained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was notdifferent at 5 min. Arteriovenous O₂ content difference waslower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 mlO₂/dl) and higher by 30 s of exercise(11.2 ± 0.7 vs. 10.8 ± 0.7 ml O₂/dl,P < 0.05). Muscle O₂was unchanged before the start of exercise but was elevated during thefirst 30 s of the transition to the second exercise bout(26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood PCO₂, pH, andlactate concentration were consistent with reduced reliance onanaerobic glycolysis at the onset of the second exercise bout. Thesedata show that limitations of muscle blood flow can restrict theadaptation of oxidative metabolism at the onset of heavy muscular exertion.

     

Spatial heterogeneity of quadriceps muscle deoxygenation kinetics during cycle exercise.

To test the hypothesis that, during exercise, substantial heterogeneity of muscle hemoglobin and myoglobin deoxygenation [deoxy(Hb + Mb)] dynamics exists and to determine whether such heterogeneity is associated with the speed of pulmonary O(2) uptake (pVo(2)) kinetics, we adapted multi-optical fibers near-infrared spectroscopy (NIRS) to characterize the spatial distribution of muscle deoxygenation kinetics at exercise onset. Seven subjects performed cycle exercise transitions from unloaded to moderate [GET) work rates and the relative changes in deoxy(Hb + Mb), at 10 sites in the quadriceps, were sampled by NIRS. At exercise onset, the time delays in muscle deoxy(Hb + Mb) were spatially inhomogeneous [intersite coefficient of variation (CV), 3~56% for GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O(2) extraction were also spatially inhomogeneous (intersite CV, 6~48% for GET) and faster (P < 0.05) than those of phase 2 pVo(2). However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pVo(2) kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of Vo(2) and O(2) delivery increase across the regions sampled.     

Cardiac output and oxygen uptake kinetics at the onset and offset of exercise

1. 1. The aim of the present study is to assess the relationship between rapidity of oxygen uptake (V_O2 and cardiac output (Q) kinetics at the transient phase of the onset and offset of exercise.

2. 2. Five healthy male subjects performed multiple rest-exercise-recovery transitions on an electrically braked ergometer, work rate was 50, 75, or 100 W for 6 min, respectively.

3. 3. V_O2 was obtained by a breath-by-breath method, and Q was measured by an impedance method during normal breath, using an ensemble averaged method.

4. 4. On transition from rest to exercise, V_O2 rapidly increased as phase I with a time constant of 7.0–7.8 s. Q also showed a similar rapid increment with a time constant of 6.3–6.8 s in phase I.

5. 5. In this phase I, V_O2 increased approx. 42–68% of steady state value and Q increased 71–84%. Thereafter, V_O2 and Q increased monoexponentially up to steady state with a time constant of 26.7–32.3 and 23.7–34.4 s, respectively.

6. 6. During recovery, V_O2 (with a time constant of 35.7–38.1 s and time delay (TD) of −1 to −2 s), while Q remained to sustain the value of steady state exercise with a couple of time delay (TD = 2–7 s), and thereafter decreased monoexponentially (with a time constant of 18.9–31.6 s).

7. 7. The stroke volume showed the similar behavior to the Q kinetics after exercise, while heart rate rapidly decreased (time constant = 10.6–21.2 s).

8. 8. It is suggested that the delayed Q kinetics after exercise might be attributable to the sustained level of venous return and that Q kinetics is not linked with V_O2 kinetics after exercise.